Feces metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA373879 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5963490_1.fastq.gz | Fastqsanger.gz | |||
| SRR5963490_2.fastq.gz | Fastqsanger.gz | |||
| SRR5963500_1.fastq.gz | Fastqsanger.gz | |||
| SRR5963500_2.fastq.gz | Fastqsanger.gz | |||
| SRR5963491_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:Gut bacterial β-glucuronidases (GUS) promote the toxic side effects of therapeutics by reactivating drugs from their inactive glucuronide conjugates. It is increasingly clear that the interindividual variability of bacterial GUS-producing species in the gut microbiota contributes to differential drug responses. Indeed, the anticancer drug irinotecan exhibits variable clinical toxicity outcomes that have been linked to interindividual differences in the composition of the gut microbiota. However, identification of the specific GUS enzymes responsible for drug metabolism in the context of the complexity of the human fecal microbiota has not been achieved. Here we pinpoint the specific bacterial GUS enzymes that reactivate SN-38, the active metabolite of irinotecan, from complex human fecal microbiota samples with activity-based protein profiling (ABPP). We identify and quantify gut bacterial GUS enzymes from human feces with ABPP-enabled proteomics and then integrate this information with ex vivo kinetics to reveal the specific GUS enzymes responsible for the reactivation of SN-38. The same ABPP approach also reveals the molecular basis for differential gut bacterial GUS inhibition between human fecal samples. Taken together, this work provides an unprecedented pipeline to identify the specific bacterial GUS enzymes responsible for drug-induced GI toxicity from the complexity of human feces, which may serve as highly precise biomarkers of clinical outcomes for irinotecan and other therapeutics.
2019-12-03 | PXD014864 | Pride
Project description:Transcriptional profiling of human breast cancer MCF-7 cells comparing control untreated cells with cells exposed to step-wise increasing doses of SN38, an active metabolite of irinotecan.
2012-03-01 | GSE27534 | GEO
Project description:The effects of several compounds on the MCF7 human adenocarcinoma mammary cell line were analysed by gene expression profiling. Tested compounds: HSP90 inhibitors: 17AAG (Tanespimycin), NVP-AUY922, NMS-E973 (cpd developed at NMS). CDK inhibitors: CDK-887 (cpd developed at NMS). Topoisomerase inhibitors: Doxorubicin, SN38 (active metabolite of Irinotecan). The MCF7 cell line was treated with the different compounds for 6 hours at a dose equal to 5 times the IC50. Untreated MCF7 cells were used as a control. Two replicates per treatment.
2010-07-14 | E-GEOD-19638 | biostudies-arrayexpress
Project description:The aim of this study was to identify biomarkers of drug response and investigate mechanisms of drug resistance to the two chemotherapeutic drugs oxaliplatin and irinotecan (active metabolite SN-38) in colorectal cancer, using a cell-based model system of drug-sensitive parental colon cancer cell lines and sub-cell lines with acquired drug resistance.
2015-03-15 | GSE42387 | GEO
Project description:Longitudinal metabolomic, metagenomic, and metaproteomic changes were measured in 27 healthy subjects supplemented with soy protein isolate (SPI, 40 g per day) for 5 days followed by GPs complexed to SPI (GP-SPI standardized to 5% GPs, 40 g per day) for 10 days. Fecal, urine, and/or fasting blood samples were collected before supplementation (day -5), after 5 days of SPI (day 0), and after 2, 4 and 10 days of GP-SPI.
2025-05-15 | PXD058659 | Pride
Project description:Objective Crohn’s Disease (CD) and Ulcerative Colitis (UC) are chronic inflammatory diseases of the gastrointestinal tract. Reliable diagnosis of these diseases requires a comprehensive examination of the patient, which include invasive endoscopy. This study assesses whether non-invasive LC-MS/MS based analysis of microbial and human proteins from feces may support the diagnosis of the diseases. Design In order to mimic a representative clinical background for this study, we investigated 17 healthy controls, 11 CD patients, 14 UC patients, also 13 Irritable Bowel Disease (IBS) patients, 8 Colon Adenoma (CA) patients, and 8 Gastric Carcinoma (GCA) patients. The proteins were extracted from the fecal samples with liquid phenol in a ball mill. Subsequently, the proteins were digested tryptically to peptides and analyzed by liquid chromatography coupled to an Orbitrap MS/MS. For protein identification and interpretation of taxonomic and functional results, the MetaProteomeAnalyzer software and the UniProtKB/SwissProt database and several metagenomes from human fecal samples were used. Results Cluster analysis and ANOSIM show a separation of healthy controls from patients with CD and UC as well as from patients with GCA. Among others, UC and CD correlated with an increase of neutrophil extracellular traps and immunoglobulins G (IgG) as well as a decrease of IgA. A specific marker metaprotein for CD was an increase of the human enzyme sucrose-isomaltase. IBS and CA patient’s fecal metaproteome showed only minor alterations. Conclusion Metaproteome analysis distinguished between patients with UC, CD and healthy controls and is therefore useful as a non-invasive tool for routine diagnostics in hospitals.
2019-03-11 | PXD010371 | Pride
Project description:Transcriptional profiling of human breast cancer MCF-7 cells comparing control untreated cells with cells exposed to step-wise increasing doses of SN38, an active metabolite of irinotecan. MCF-7 cell clones were established by a limiting dilution method. SN38-sensitive MCF-7 clone (Clone 3) was used for further analyses. MCF-7/SNR cells were established by continuously exposing this clone to SN38 with stepwise increasing concentrations ranging from 0.5 ng/mL to 50 ng/mL over a period of six months. MCF-7/SNR cells were maintained in the presence of 50 ng/mL SN38 until 24 h prior to any experiment. Total RNA was extracted from MCF-7 and MCF-7/SNR cells for cDNA microarray analysis.
2012-03-01 | E-GEOD-27534 | biostudies-arrayexpress